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Siglec-7 可恢复糖尿病患者胰岛中的β细胞功能和生存，并减轻炎症反应。

Siglec-7 restores β-cell function and survival and reduces inflammation in pancreatic islets from patients with diabetes.

机构信息

Centre for Biomolecular Interactions Bremen, University of Bremen, Germany.

Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences) and University Medical Center Utrecht, Cancer Genomics Netherlands, Utrecht, The Netherlands.

出版信息

Sci Rep. 2017 Apr 5;7:45319. doi: 10.1038/srep45319.

DOI:10.1038/srep45319
PMID:28378743
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5381285/
Abstract

Chronic inflammation plays a key role in both type 1 and type 2 diabetes. Cytokine and chemokine production within the islets in a diabetic milieu results in β-cell failure and diabetes progression. Identification of targets, which both prevent macrophage activation and infiltration into islets and restore β-cell functionality is essential for effective diabetes therapy. We report that certain Sialic-acid-binding immunoglobulin-like-lectins (siglecs) are expressed in human pancreatic islets in a cell-type specific manner. Siglec-7 was expressed on β-cells and down-regulated in type 1 and type 2 diabetes and in infiltrating activated immune cells. Over-expression of Siglec-7 in diabetic islets reduced cytokines, prevented β-cell dysfunction and apoptosis and reduced recruiting of migrating monocytes. Our data suggest that restoration of human Siglec-7 expression may be a novel therapeutic strategy targeted to both inhibition of immune activation and preservation of β-cell function and survival.

摘要

慢性炎症在 1 型和 2 型糖尿病中都起着关键作用。在糖尿病环境中，胰岛内细胞因子和趋化因子的产生导致β细胞衰竭和糖尿病进展。确定既能防止巨噬细胞活化和浸润胰岛，又能恢复β细胞功能的靶点，对于有效的糖尿病治疗至关重要。我们报告说，某些唾液酸结合免疫球蛋白样凝集素（Siglecs）以细胞类型特异性的方式在人胰腺胰岛中表达。Siglec-7 在β细胞上表达，并在 1 型和 2 型糖尿病以及浸润的活化免疫细胞中下调。在糖尿病胰岛中过表达 Siglec-7 可减少细胞因子，防止β细胞功能障碍和细胞凋亡，并减少迁移单核细胞的募集。我们的数据表明，恢复人 Siglec-7 的表达可能是一种新的治疗策略，靶向于抑制免疫激活和保护β细胞功能和存活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/357e4aaa3d64/srep45319-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/e08c9f933ee6/srep45319-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/db2ec3b4e3c4/srep45319-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/93d5b4694c2a/srep45319-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/357e4aaa3d64/srep45319-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/e08c9f933ee6/srep45319-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/205d0d78c999/srep45319-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/cc800fdaacf8/srep45319-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/db2ec3b4e3c4/srep45319-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/93d5b4694c2a/srep45319-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603d/5381285/357e4aaa3d64/srep45319-f6.jpg

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